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Origin of the Aschoff Body Ann Rheum Dis: first published as 10.1136/ard.22.3.127 on 1 May 1963. Downloaded from Ann. rheum. Dis. (1963), 22, 127. ORIGIN OF THE ASCHOFF BODY BY BERNICE G. WEDUM Rheumatic Fever Study, Frederick, Maryland AND JOHN W. McGUIRE Photography Section, Medical Arts and Photography Branch, Division of Research Services, National Institutes of Health, Bethesda, Md. Rheumatic fever has been compared with tuber- students of rheumatic fever for the next 150 years. culosis (Thorel, 1910; Fahr, 1930), Hodgkin's Ludwig Aschoff directed his attention to this disease (Aschoff and Tawara, 1906; Gross, Loewe, problem in his first paper (1904), seeking for evidence and Eliasoph, 1929), and hypersensitivity reactions that the conduction system of the heart was affected (Swift, 1924; Klinge, 1933). The ultimate, com- in acute rheumatism and was responsible for the plete explanation of its pathogenesis must explain functional disorder, an idea previously advanced by why it has presented such varying aspects to such Peter (1891). Aschoff found no evidence to support profound students of the disease. The present study such a theory in the three cases which were the concerns the nature of its most specific pathological subject of his first paper, but Aschoff and Tawara manifestations, the Aschoff body of the heart. (1906), in their monograph on the failing heart, copyright. Evidence is presented that the Aschoff body is described one case with considerable involvement of derived from the larger lymphatic vessels of the the bundle of Hiss. They came to the conclusion heart; the central core, which may be present, is that the basic disorder was an anaemic necrosis of composed of precipitated lymph and necrotic the myocardium caused by perivasculitis of the protoplasm. These granulomata form at points of blood vessels supplying the muscle. They had mechanical stress, especially under the endo- found in the adventitia of the blood vessels "peculiar cardium and in the region of the intramyocardial nodules which were specific for rheumatic carditis http://ard.bmj.com/ coronary arteries. Damage to cardiac muscle and ... developed by an aggregation of conspicuously connective tissue is secondary to the lymphoedema large elements with one or more abnormally large, which follows obstruction of the lymphatic vessels slightly indented or polymorphous nuclei. The by the proliferating endothelial cells. It is most aggregation of these cells often takes the form of prominent at points of mechanical trauma, notably a fan or rosette. The periphery is formed by the at the point of closure of the heart valves, where large nuclei, and the centre by apparently necrotic form. protoplasm, staining here weaker and somewhat vegetations on September 28, 2021 by guest. Protected The existence of a rheumatism of the heart was different" (Aschoff, 1904). first clearly defined by Dundas (1809), although The greatness of Aschoff's contribution lies not Jenner (1789) had written an account of the associa- only in his recognition of a granuloma specific for tion (his manuscript was subsequently lost), and it rheumatic carditis, but also in his recognition that had also been mentioned by Pitcairn (1797) and the damage to the myocardium was in some manner Odier (1806). In his second edition, Odier (1811) secondary to the specific lesion in the connective reported two cases of rheumatic adhesive peri- tissue. Poynton (1899) had also appreciated that carditis in a footnote, and concluded, "But what is "the function of cardiac muscle is damaged in a difficult to understand is that this complete adher- peculiar way, rather than destroyed by the rheumatic ence of the two organs which are naturally detached poison". (The term "peculiar disease of the heart" one from the other did not in any way disturb the had been used by Dundas (1809), Aschoff wrote of circulation." "peculiar nodules", and years later MacCallum Thus at the beginning of the 19th century the (1924) was to mention "lymphatic channels filled question was asked why the heart failed in rheu- with lymphocytes which form a peculiar and rather matic carditis, and this question was to occupy conspicuous feature", and that rheumatic fever was 127 Ann Rheum Dis: first published as 10.1136/ard.22.3.127 on 1 May 1963. Downloaded from 128 ANNALS OF THE RHEUMATIC DISEASES caused by a specific infectious agent of some concerned with the pathology of rheumatic heart peculiar kind (MacCallum, 1925). In identical disease, assuming that the Aschoff cell was derived language these able students of the disease expressed from some type of connective tissue cell. Interest their awareness of something unusual and not centred chiefly in the mode of formation of this cell, heretofore encountered in rheumatic carditis.) whether by mitotic or amitotic division of nuclei, With only a few dissenting voices, the specificity which would suggest a mechanism of pathogenesis of the granuloma described by Aschofffor rheumatic involving DNA, or by fusion, which would suggest carditis was widely accepted. The exact origin of an alteration in the cell membrane. Studies on the the characteristic giant cell remained in doubt. aetiology of rheumatic fever in progress in our The majority considered it to be some type of con- laboratory included the use of tissue culture of left nective tissue or endothelial cell (Aschoff, 1904, auricular appendages obtained at surgery for mitral 1906; Geipel, 1905; Fraenkel, 1912; Swift, 1924; stenosis. With the appearance of the monograph Letulle, Bezanqon, and Weil, 1926; Clawson, Bell, by Murphy (1960), suggesting the origin of the and Hartzell, 1926). A few (Huzella, 1914; Whit- Aschoff cell from the myofibre itself, it seemed man and Eastlake, 1920; Murphy, 1960) considered essential to re-investigate this question in order to be this giant cell to be derived from the myocardial certain that our experimental approach was sound. fibre itself. Others, while holding to the view that Connective tissue cells migrate in tissue culture, but the Aschoff cell was a connective tissue cell, believed the myofibre does not. that giant cells could also arise from the myocardium (Saigo, 1908; Letulle, Bezanqon, and Weil, 1926; Wagner and Tedeschi, 1955). The views of many Present Investigations investigators have been summarized by McEwen It seemed that the pathology of rheumatic (1932). carditis would be seen most clearly in patients dying The important question debated during the next in the course of a first attack of rheumatic fever. 25 years was whether the central core of the An effort was made, therefore, to obtain material granuloma described so carefully by Aschoff as from as many early cases as possible. Such cases copyright. "necrotic protoplasm" was in fact the primary are rare, but it was possible to collect six with three lesion. Klinge (1933), in his monumental study of additional cases of children of similar age dying of all forms of rheumatism, concluded that exudation causes unrelated to the heart to serve as controls was the primary process, consisting of a specific (Table, overleaf, p. 129). Details are given in the type of damage to collagen fibrils. He also stated, Appendix, p. 139. however, that proliferation and exudation might Method occur simultaneously and, in agreement with http://ard.bmj.com/ Talalajew (1929), that perhaps in the heart the The co-author (J.W.McG.) pointed out that primary process was cellular proliferation. Aschoff details could be seen on large colour transparencies (1939) published pictures showing undamaged which were not apparent under the microscope. fibrils in early Aschoff bodies and maintained that A series of eighty 8 x 10-inch colour transparencies, rheumatic carditis was essentially a proliferative some at magnifications as high as 2,450, was taken disease of cells. Rheumatic fever, nevertheless, of the sections, exploring each system of the heart. became known as a collagen disease and the search It was then to the transparencies, possible examine on September 28, 2021 by guest. Protected for the aetiologic agent became an inquiry into the using a view box, and to study them over long mechanism by which this alteration in collagen was periods, sometimes with the aid of a hand lens. produced. Still unanswered was the question how myocardial function was so profoundly altered as a result of connective tissue damage. Results For more extensive reviews the writings of Itard In the course of these studies a dilated lymphatic (1824), Eulenberg (1854), Besnier (1877), Janot vessel, its endothelial lining cells exhibiting unusual (1902), Gallavardin (1908), Jacki (1919-20), Bezan- features in that they resembled early Aschoff cells, (on and Well (1926), Sacks (1926), Paul (1928), was noted between two blood vessels (Figs 1 and 2, Clawson (1929), Klinge (1933), Gross and Ehrlich opposite). A search for lymphatic vessels in (1934), Wilson (1940), Baggenstoss (1953), Murphy sections of normal hearts revealed none which could (1943, 1960) should be consulted, together with the be discerned, nor were there any special stains section on rheumatic fever in the Rheumatism and available to differentiate lymphatic vessels from Arthritis Review (1962). surrounding connective tissue. For the past 20 years the writer (B.G.W.) has been IAn inquiry into the anatomy of the lymphatic Ann Rheum Dis: first published as 10.1136/ard.22.3.127 on 1 May 1963. Downloaded from ORIGIN OF THE ASCHOFF BODY -a re' - - ' li'w }: 1~~~0t - A- -'~~~~~~~1-a "'aaroorrwr 5-,s -'. It.t Caer. x 50 A~~~ vessel between two blood vessel in 1 under power, showin Fig. 1.-Lymphatic vessels,showsng swelling Fig. 2.-Lymphatic Fig. higher copyright. of endothelial cells with central condensation of nuclear chromatin. details of formation of early Aschoff cells. Case 1. x 1,500. Case 1. x 150. f _ _, d'- http://ard.bmj.com/ on September 28, 2021 by guest. Protected Fig. 10.-Aschoff body forming from lymphatic channel cut in cross- Fig.
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